Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Farkas, Eszter; Jong, G.I. de; Vos, Rob A. I. de; Steur, Ernst N.H. Jansen; Luiten, P.G.M.

doi:10.1007/s004010000195

Cited by 187 publications

(141 citation statements)

References 41 publications

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“…Others reported similar capillary deformities found in post mortem AD material [30,47]. Our own studies also gathered evidence that the cerebrocortical capillaries of AD and other dementing patients suffer considerable pathological changes [15,16]. Electron microscopic analysis of post mortem samples from the cingulate cortex demonstrated that the capillary basement membrane was a preferential site of ultrastructural degradation in AD and Parkinson's disease with dementia (PDd).…”

Section: Reduced Cbf and Cerebral Capillary Ultrastructuresupporting

confidence: 73%

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Farkas

Vos

Steur

et al. 2000

Neurobiology of Aging

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Section: Reduced Cbf and Cerebral Capillary Ultrastructuresupporting

confidence: 73%

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Farkas

Vos

Steur

et al. 2000

Neurobiology of Aging

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“…7 More specifically, neuroimaging findings indicate white matter hyperintensities, cerebrovascular lesions, and cerebral amyloid angiopathy (CAA). 8 Other ultrastructural abnormalities to the microvasculature associated with small-vessel disease, and exacerbated by aging, include capillary wall deterioration and the accumulation of erythrocytes, 9 basement membrane thickening, and pericyte degeneration, 10 resulting in blood-brain barrier (BBB) permeability 11 and vascular cognitive impairment (VCI). Vascular cognitive impairment is a broad term that encompasses cognitive deficits associated with vascular disease, ranging from mild-to-severe cognitive impairment including VaD.…”

Section: Introductionmentioning

confidence: 99%

The neuropathology and cerebrovascular mechanisms of dementia

Raz

Knoefel

Bhaskar

2015

J Cereb Blood Flow Metab

349

284

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The prevalence of dementia is increasing in our aging population at an alarming rate. Because of the heterogeneity of clinical presentation and complexity of disease neuropathology, dementia classifications remain controversial. Recently, the National Plan to address Alzheimer's Disease prioritized Alzheimer's disease-related dementias to include: Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, vascular dementia, and mixed dementias. While each of these dementing conditions has their unique pathologic signature, one common etiology shared among all these conditions is cerebrovascular dysfunction at some point during the disease process. The goal of this comprehensive review is to summarize the current findings in the field and address the important contributions of cerebrovascular, physiologic, and cellular alterations to cognitive impairment in these human dementias. Specifically, evidence will be presented in support of small-vessel disease as an underlying neuropathologic hallmark of various dementias, while controversial findings will also be highlighted. Finally, the molecular mechanisms shared among all dementia types including hypoxia, oxidative stress, mitochondrial bioenergetics, neuroinflammation, neurodegeneration, and bloodbrain barrier permeability responsible for disease etiology and progression will be discussed.

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“…A link between AD and cerebrovascular disease, especially of the white matter, may be capillary degeneration in AD, leading t o metabolic derangement (Farkas et al, 2000;de la Torre, 2000). Aging and AD also show fibrohyaline arteriolosclerosis that may lead to an impaired autoregulation; and amyloid angiopathy of the penetrator shaft may be another cause of vessel dysregulation.…”

Section: Resultsmentioning

confidence: 99%

Vascular Burden of the White Matter

Brun

2003

Int. Psychogeriatr.

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ABSTRACT. In cerebrovascular disease of all kinds, the white matter bears a heavy burdenparticularly in the early and late periods of life, The infarcts are of the complete and incomplete type, the latter accompanying and extending the white-matter damage of the former. Complete infarcts are mainly caused by vascular occlusions. Incomplete infarcts are mainly due to hypoperfusion, wherein pathogenic factors are, above all, different types of angiopathies leading to an inadequate autoregulatory response in the event of an episodic or more longstanding hypotension, acting as an etiological factor through hypoperfusion. There is growing consensus that white-matter lesions affect brain function. Correlation with symptoms and understanding of mechanisms behind the lesions would gain from more precise diagnostics as to tracts involved.

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Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

Cited by 187 publications

References 41 publications

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

Are Alzheimer’s disease, hypertension, and cerebrocapillary damage related?☆

The neuropathology and cerebrovascular mechanisms of dementia

Vascular Burden of the White Matter

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